Current Data on Dietary Sodium, Arterial Structure and Function in Humans: A Systematic Review.

BACKGROUND: Subclinical arterial damage (SAD) (arteriosclerosis, arterial remodeling and atheromatosis) pre-exists decades before cardiovascular disease (CVD) onset. Worldwide, sodium (Na) intake is almost double international recommendations and has been linked with CVD and death, although in a J-shape manner. Studies regarding dietary Na and major types of SAD may provide pathophysiological insight into the association between Na and CVD. OBJECTIVES: Systematic review of data derived from observational and interventional studies in humans, investigating the association between dietary Na with (i) atheromatosis (arterial plaques); (ii) arteriosclerosis (various biomarkers of arterial stiffness); (iii) arterial remodeling (intima-media thickening and arterial lumen diameters). DATA SOURCES: Applying the PRISMA criteria, the PubMed and Scopus databases were used. RESULTS: 36 studies were included: 27 examining arteriosclerosis, four arteriosclerosis and arterial remodeling, three arterial remodeling, and two arterial remodeling and atheromatosis. CONCLUSIONS: (i) Although several studies exist, the evidence does not clearly support a clinically meaningful and direct (independent from blood pressure) effect of Na on arterial wall stiffening; (ii) data regarding the association of dietary Na with arterial remodeling are limited, mostly suggesting a positive trend between dietary Na and arterial hypertrophy but still inconclusive; (iii) as regards to atheromatosis, data are scarce and the available studies present high heterogeneity. Further state-of-the-art interventional studies must address the remaining controversies.

Prediction of Acute Glomerular Filtration Rate Reductions Following Renin-angiotensin System Blockade in Chronic Kidney Disease: A Possible Application of Ultrasonography in Clinical Practice.

Objective Renal arteriolosclerosis is a risk factor for acute reductions in the glomerular filtration rate (GFR) when renin-angiotensin system (RAS) inhibitors are administered. Renal arteriolosclerosis can be detected by an increase in the resistive index (RI) on Doppler ultrasonography. The purpose of the present study is to determine whether or not the RI can predict acute GFR reductions following RAS blockade in chronic kidney disease (CKD). Methods We surveyed all CKD patients who were hospitalized in Otemae Hospital from January 2008 to December 2017. One hundred and eight patients who had been newly treated with RAS inhibitors were able to be followed for 14 weeks. The end point was an acute reduction in the GFR, defined as a decrease of ≥30%. Results Twenty-three of the 108 patients presented with acute GFR reductions. The cumulative probability of acute GFR reductions was 3.3% and 53% in patients with RI ≤0.70 and RI >0.70, respectively (p<0.001). A univariate Cox proportional-hazards analysis showed that the RI, age, GFR, systolic blood pressure, urinary protein excretion, diabetic kidney disease, coronary artery disease, and use of diuretics were significant variables. Multivariate hazard ratios were calculated from the RI and three established variables (age, GFR, diuretics), and the RI and use of diuretics were shown to be significant risk factors for acute GFR reductions. Conclusion These results suggest that an increase in the RI, as well as the use of diuretics, may be risk factors for acute GFR reductions following RAS blockade.

Potential Effects of Desalinated Seawater on Arteriosclerosis in Rats.

To evaluate the potential risk of arteriosclerosis caused by desalinated seawater, Wistar rats were provided desalinated seawater over a 1-year period, and blood samples were collected at 0, 90, 180, and 360 days. Blood calcium, magnesium, and arteriosclerosis-related indicators were investigated. Female rats treated with desalinated seawater for 180 days showed lower magnesium levels than the control rats (P < 0.05). The calcium and magnesium levels in female rats and the magnesium level in male rats were lower than the levels in the controls, following treatment with desalinated seawater for 360 days (P < 0.05). Blood levels of arteriosclerosis-related lipid peroxidation indicators and C-reactive protein (CRP) in the treatment group did not differ from those in the controls. The levels of lipid peroxidation indicators and CRP in rats were not significantly affected by drinking desalinated seawater, and no increase in risk of arteriosclerosis was observed.

Effect of sirolimus on arteriosclerosis induced by advanced glycation end products via inhibition of the ILK/mTOR pathway in kidney transplantation recipients.

To investigate the effect and related mechanism of sirolimus (SRL) in arteriosclerosis(AS) induced by advanced glycation end products (AGEs) in kidney transplantation recipients (KTRs). Human kidney tissues from KTRs before and after treatment with SRL were assessed by hematoxylin-eosin and immunohistochemical staining. Rat vascular smooth muscle cells (VSMCs) were treated with AGEs and/or SRL. The expressions of α-smooth muscle actin (α-SMA), osteopontin (OPN), actinin-associated LIM protein (ALP), proliferating cell nuclear antigen (PCNA), integrin-linked kinase (ILK) and the mTOR signaling pathway proteins were examined using western blot assay. Cytosolic calcium present in VSMCs was also measured by the calcium assay kit and von Kossa staining assay. The expression of α-SMA was remarkably higher while OPN expression was significantly lower in recipients with AS after they were administered SRL. Rat VSMCs treated with AGEs exhibited significantly lower expression of α-SMA and overexpression of OPN, ALP and PCNA than the other groups. In contrast, the expression of α-SMA was significantly higher while the expression of OPN, ALP and PCNA was significantly lower in VSMCs treated with both AGEs and SRL. Moreover, the ILK/mTOR signaling pathway was activated in rat VSMCs treated with AGEs, while treatment with AGEs and SRL led to significant inhibition of the ILK/mTOR signaling pathway. AGEs play a critical role in the development and progression of AS after kidney transplantation, but SRL can reverse these effects and therefore slow down the development of AS through inhibition of the ILK/mTOR signaling pathway.

Clinical Search for Undiagnosed Mesenteric Phlebosclerosis at Outpatient Departments Specializing in Herbal (Kampo) Medicine.

OBJECTIVE: Mesenteric phlebosclerosis (MP) is a disease characterized by calcification of the mesenteric vein, which causes chronic mesenteric ischemia. Recently, the long-term intake of gardenia fruit ('Sanshishi' in Japanese) has been attracting attention as a possible cause. Usually, only advanced, severe MP cases get reported. However, we suspected that some latent cases of this disease may exist. We performed this study in order to determine the prediagnostic cases at our outpatient departments of herbal (Kampo) medicine, with particular attention paid to the initial changes, such as any slight color change of the colon, as shown in colonoscopy. METHODS: We recommend colonoscopy and computed tomography (CT) scans for patients with a long-term history of taking herbal medicines containing gardenia fruit. Clinical examinations were performed upon receiving patients' consent from December 2013 to November 2014. RESULTS: Of the 103 patients who took gardenia fruit long-term, 29 agreed to be checked for MP. 14 patients underwent colonoscopy. Four patients were confirmed to have MP due to the presence of fibrotic deposition of the colonic membrane on histological inspection. Twenty-one patients underwent abdominal CT screening. Characteristic calcification of the mesenteric vein was observed on CT scans in 2 patients. All 4 MP patients took Kampo formulas containing gardenia fruit for more than 6.8 years. The other patients did not develop MP, despite long-term gardenia fruit intake. CONCLUSION: We detected the latent and undiagnosed MP cases. All diagnoses were made while paying careful attention to any slight changes in colonoscopy and CT scans.

Melatonin Attenuates Aortic Endothelial Permeability and Arteriosclerosis in Streptozotocin-Induced Diabetic Rats: Possible Role of MLCK- and MLCP-Dependent MLC Phosphorylation.

The development of diabetic macrovascular complications is a multifactorial process, and melatonin may possess cardiovascular protective properties. This study was designed to evaluate whether melatonin attenuates arteriosclerosis and endothelial permeability by suppressing the myosin light-chain kinase (MLCK)/myosin light-chain phosphorylation (p-MLC) system via the mitogen-activated protein kinase (MAPK) signaling pathway or by suppressing the myosin phosphatase-targeting subunit phosphorylation (p-MYPT)/p-MLC system in diabetes mellitus (DM). Rats were randomly divided into 4 groups, including control, high-fat diet, DM, and DM + melatonin groups. Melatonin was administered (10 mg/kg/d) by gavage for 12 weeks. The DM significantly increased the serum fasting blood glucose and lipid levels, as well as insulin resistance and endothelial dysfunction, which were attenuated by melatonin therapy to various extents. Importantly, the aortic endothelial permeability was significantly increased in DM rats but was dramatically reversed following treatment with melatonin. Our findings further indicated that hyperglycemia and hyperlipidemia enhanced the expressions of MLCK, p-MYPT, and p-MLC, which were partly associated with decreased membrane type 1 expression, increased extracellular signal-regulated kinase (ERK) phosphorylation, and increased p38 expression. However, these changes in protein expression were also significantly reversed by melatonin. Thus, our results are the first to demonstrate that the endothelial hyperpermeability induced by DM is associated with increased expressions of MLCK, p-MYPT, and p-MLC, which can be attenuated by melatonin at least partly through the ERK/p38 signaling pathway.

Dietary ellagic acid improves oxidant-induced endothelial dysfunction and atherosclerosis: role of Nrf2 activation.

BACKGROUND: Oxidative stress-induced vascular endothelial cell injury is a major factor in the pathogenesis of atherosclerosis. Several evidences indicate that ellagic acid (EA), a phenolic compound, contributes to cardiovascular health. This study was to investigate the effects of EA on endothelial dysfunction and atherosclerosis via antioxidant-related mechanisms. METHODS: In animal studies, wild-type (WT) C57BL/6 mice and apolipoprotein E-deficient mice (ApoE(-/-)) mice were fed: a high-fat (21%) diet (HFD) or a HFD plus with EA (HFD+EA), for 14weeks. Vascular reactivity was studied in mice aortas. The effect of EA in human umbilical vein endothelial cells (HAECs) exposed to hypochlorous acid (HOCl) was also investigated. RESULTS: Compared with animals on HFD alone, EA attenuated atherosclerosis in WT mice. In aortic rings from two mice models, EA significantly improved endothelium-dependent relaxation and attenuated HOCl-induced endothelial dysfunction. Besides, EA significantly improved nitric oxide synthase activity, antioxidant capacity and markers of endothelial dysfunction in plasma. Western blot analysis showed that EA increased NF-E2-related factor 2 (Nrf2) and heme oxygenase-1(HO-1) expression in the aortas (P<0.05). In a separate experiment, EA did not protect against HOCl-induced endothelial dysfunction in arteries obtained from Nrf2 gene knockout mice compared with WT mice. In HAECs, EA prevented HOCl-induced cellular damage and induced HO-1 protein expression, and these effects markedly abolished by the siRNA of Nrf2. CONCLUSIONS: Our results provide further support for the protective effects of dietary EA particularly oxidant-induced endothelial dysfunction and atherosclerosis partly via Nrf2 activation.

Lipoic acid, but not tempol, preserves vascular compliance and decreases medial calcification in a model of elastocalcinosis.

Vascular calcification decreases compliance and increases morbidity. Mechanisms of this process are unclear. The role of oxidative stress and effects of antioxidants have been poorly explored. We investigated effects of the antioxidants lipoic acid (LA) and tempol in a model of atherosclerosis associated with elastocalcinosis. Male New Zealand white rabbits (2.5-3.0 kg) were fed regular chow (controls) or a 0.5% cholesterol (chol) diet+104 IU/day vitamin D2 (vitD) for 12 weeks, and assigned to treatment with water (vehicle, n=20), 0.12 mmol·kg-1·day-1 LA (n=11) or 0.1 mmol·kg-1·day-1 tempol (n=15). Chol+vitD-fed rabbits developed atherosclerotic plaques associated with expansive remodeling, elastic fiber disruption, medial calcification, and increased aortic stiffness. Histologically, LA prevented medial calcification by ∼60% and aortic stiffening by ∼60%. LA also preserved responsiveness to constrictor agents, while intima-media thickening was increased. In contrast to LA, tempol was associated with increased plaque collagen content, medial calcification and aortic stiffness, and produced differential changes in vasoactive responses in the chol+vitD group. Both LA and tempol prevented superoxide signals with chol+vitD. However, only LA prevented hydrogen peroxide-related signals with chol+vitD, while tempol enhanced them. These data suggest that LA, opposite to tempol, can minimize calcification and compliance loss in elastocalcionosis by inhibition of hydrogen peroxide generation.

Lipoic acid, but not tempol, preserves vascular compliance and decreases medial calcification in a model of elastocalcinosis

Vascular calcification decreases compliance and increases morbidity. Mechanisms of this process are unclear. The role of oxidative stress and effects of antioxidants have been poorly explored. We investigated effects of the antioxidants lipoic acid (LA) and tempol in a model of atherosclerosis associated with elastocalcinosis. Male New Zealand white rabbits (2.5-3.0 kg) were fed regular chow (controls) or a 0.5% cholesterol (chol) diet+104 IU/day vitamin D2 (vitD) for 12 weeks, and assigned to treatment with water (vehicle, n=20), 0.12 mmol·kg-1·day-1 LA (n=11) or 0.1 mmol·kg-1·day-1 tempol (n=15). Chol+vitD-fed rabbits developed atherosclerotic plaques associated with expansive remodeling, elastic fiber disruption, medial calcification, and increased aortic stiffness. Histologically, LA prevented medial calcification by ∼60% and aortic stiffening by ∼60%. LA also preserved responsiveness to constrictor agents, while intima-media thickening was increased. In contrast to LA, tempol was associated with increased plaque collagen content, medial calcification and aortic stiffness, and produced differential changes in vasoactive responses in the chol+vitD group. Both LA and tempol prevented superoxide signals with chol+vitD. However, only LA prevented hydrogen peroxide-related signals with chol+vitD, while tempol enhanced them. These data suggest that LA, opposite to tempol, can minimize calcification and compliance loss in elastocalcionosis by inhibition of hydrogen peroxide generation.

Protease inhibitor treatment effect on aortic stiffness in normotensive patients with human immunodeficiency virus infection.

OBJECTIVES: Human immunodeficiency virus (HIV) infection and protease inhibitor (PI)-based antiretroviral treatment might increase large artery (aortic) stiffness compared with healthy untreated controls. To clarify the role of PI therapy in the progression of subclinical arteriosclerosis in patients with HIV, we investigated the impact of PI treatment on arterial stiffness. METHODS AND RESULTS: In our single-centre, cross-sectional study, normotensive male HIV patients free from overt cardiovascular disease received PI treatment (n=60) or no PI treatment (n=42). The PI group had a significantly higher pulse wave velocity (PWV) than the PI-free group (9.0 ± 1.4 vs. 8.1 ± 1.3m/s; P=0.016). There was a significant positive correlation between age and PWV in the PI-free group (R(2) 0.310; P<0.0001) and, to a lesser extent, in the PI group (R(2) 0.181; P<0.0001). PI treatment was associated with a significant increase in the adjusted slope of the curve relating age to PWV as compared with no PI treatment. CONCLUSIONS: In normotensive HIV patients, PI treatment significantly increases both aortic stiffness and the positive correlation between PWV and age. Aortic stiffness predicts cardiovascular mortality, thus these results provide new insight on the relationship between PI treatment, mechanical arteriosclerotic and cardiovascular risk.

[Exposure to nanoparticle-rich diesel exhaust may cause liver damage].

Diesel exhaust (DE) is one of the air pollutants in the world, and exposure to DE is an environmental health concern. Most studies amongst the limited number of studies on hepatotoxicity have focused on genotoxicity or mutagenicity. However, DE exposure may cause liver damage because one prospective study suggests that DE exposure is associated with increased mortality due to arteriosclerosis and cirrhosis of the liver. Peroxisome proliferator-activated receptor (PPAR) α plays a role in the regulation of lipid homeostasis and inflammation and thereby may be involved in the progression of atherosclerosis. We investigated whether nanoparticle-rich diesel exhaust (NR-DE) affects the liver and how PPARα is involved in the NR-DE induced effects. We report these results briefly in this minireview. Our results suggest NR-DE-induced hepatic inflammation and dyslipidemia. PPARα may be involved in the development of these disorders.

Antiatheromatic effects of insulin.

Despite numerous publications according to which insulin promotes atherosclerosis, there are many observations in the last fifteen years suggesting that insulin has antiatherogenic properties. Insulin has vasodilatory, antithrombotic and anti-inflammatory effects. A good glycemic control contributes to the maximum efficiency of antiatherogenic action of insulin. Insulin resistance promotes the atherosclerotic process because of diminished insulin action and not because of hyperinsulinemia, since insulin secretion is getting lower during the years in type 2 diabetes.

Motor complications, levodopa metabolism and progression of Parkinson's disease.

INTRODUCTION: Oxidative stress is an essential component of neuronal death in Parkinson's disease (PD). Clinically, progression of PD is also characterised by onset of motor complications (MC). MC results from the peripheral and central degree of fluctuations of levodopa (LD) and of dopamine. AREAS COVERED: This review highlights aspects of LD and dopamine metabolism in chronic neurodegeneration in PD. A Medline search (terms: homocysteine, LD, PD, progression [from 2000 onwards]) was performed and considered preclinical and clinical investigations. The author discusses pharmacokinetic and metabolic aspects of chronic LD administration in PD patients and provides a therapeutic concept to reduce probable PD accelerating consequences of chronic LD application. EXPERT OPINION: The author suggests that the future 'ideal' oral LD therapy should be homocysteine-reducing, methyl-group-donating, oxidative-stress-decreasing and antiglutamatergic while also allowing continuous delivery to the brain. This may slow the progression of PD and delay the onset of MC, both of which represent unmet needs in the treatment of PD patients.

Enfermedad cardiovascular en el paciente infectado por el virus de la inmunodeficiencia humana / Cardiovascular risk in the human immunodeficiency virus infected patient

ResumenCon la introducción del tratamiento antirretroviral de alta eficacia, las enfermedades arterioscleróticas han ganado importancia como causa de morbilidad y mortalidad en personas infectadas por el virus de la inmunodeficiencia humana (VIH). A continuación, se examinará el riesgo de enfermedades cardiovasculares en personas infectadas por el VIH y se comparará con la población no infectada. Se expondrán las contribuciones relativas al huésped, a la infección por el VIH, y la terapia antirretroviral a la luz de los conocimientos actuales.ResumenEl riesgo absoluto de desarrollar una enfermedad cardiovascular en pacientes infectados por el VIH que reciben terapia antirretroviral es bajo. Sin embargo, este riesgo esta aumentado en comparación con el riesgo que tienen las personas no infectadas. Este hecho es sustancialmente debido a una mayor prevalencia de los factores de riesgo cardiovasculares tradicionales que son en su mayoría dependientes del huésped. La infección por el VIH puede contribuir tanto directamente, a través de la activación inmune y la inflamación, e indirectamente a través de la inmunodeficiencia que provoca el virus. El tipo de tratamiento antirretroviral, aunque en menor medida que la infección por VIH, puede contribuir a aumentar el riesgo cardiovascular a través de sus efectos metabólicos y también debido a los cambios que se producen en la composición corporal de la grasa.ResumenLa prevención de la enfermedad cardiovascular en los pacientes infectados por el VIH constituye un aspecto importante.(..) (AU)

AbstractWith the introduction of effective antiretroviral therapy (ART), cardiovascular disease has gained importance as a cause of morbidity and mortality in HIV-infected persons. Herein, we will study the risk of cardiovascular disease in HIV-infected persons compared to the non-infected population. The relative contributions regarding the host, HIV infection and antiretroviral therapy will be presented in the light of current knowledge. The absolute risk of developing cardiovascular disease in HIV-infected patients receiving antiretroviral therapy is low. However, this risk is increasing compared to the risk in uninfected persons. This fact is substantially due to a higher prevalence of underlying traditional cardiovascular risk factors that are mostly host-dependent. HIV infection may contribute both directly through immune activation and inflammation and indirectly through immunodeficiency. The type of antiretroviral treatment, also to a lesser degree than HIV infection, may also contribute through its impact on metabolic effects and also because of the changes produced in body fat parameters.AbstractPrevention of cardiovascular disease in HIV-infected patients should be standard care.AbstractThe traditional risk factors should be investigated and aggressively treated whenever possible, since they play a major role in the development of cardiovascular disease. Antiretroviral therapy should be initiated earlier in patients with high cardiovascular risk. From a purely cardiovascular perspective, the benefits of ART, regardless of the drugs used, clearly outweigh any potential risk (AU)

Long-term exposure to air pollution and vascular damage in young adults.

BACKGROUND: Long-term exposure to ambient air pollution has recently been linked to atherosclerosis and cardiovascular events. There are, however, very limited data in healthy young people. We examined the association between air pollutants and indicators of vascular damage in a cohort of young adults. METHODS: We used data from the Atherosclerosis Risk in Young Adults study. We estimated exposure to nitrogen dioxide (NO2), particulate matter less than 2.5 microm in aerodynamic diameter (PM2.5), black smoke, sulfur dioxide (SO2), and various traffic indicators for participants' 2000 home addresses. Exposure for the year 2000 was estimated by land-use regression models incorporating regional background annual air pollution levels, land-use variables, population densities, and traffic intensities on nearby roads. Outcomes were common carotid artery intima-media thickness (n = 745), aortic pulse wave velocity (n = 524), and augmentation index (n = 729). RESULTS: Exposure contrasts were substantial for NO2, SO2, and black smoke (5th-95th percentiles = 19.7 to 44.9, 2.5 to 5.2, and 8.6 to 19.4 microg/m3, respectively) and smaller for PM2.5 (16.5 to 19.9 microg/m3). The variability of carotid artery intima-media thickness was less than for pulse wave velocity and especially augmentation index (5-95th percentiles = 0.42 to 0.58 mm, 4.9 to 7.4 m/s and -12.3% to 27.3%, respectively). No associations were found between any of the pollutants or traffic indicators and carotid artery intima-media thickness, although PM2.5 effect estimates were in line with previous studies. We observed a 4.1% (95% confidence interval = 0.1% to 8.0%) increase in pulse wave velocity and a 37.6% (2.2% to 72.9%) increase in augmentation index associated with a 25 microg/m3 increase in NO2, and a 5.3% (0.1% to 10.4%) increase in pulse wave velocity with a 5 microg/m3 increase in SO2. PM2.5 and black smoke were not associated with either of these 2 outcomes. CONCLUSIONS: Air pollution may accelerate arterial-wall stiffening in young adults. Small outcome variability and lack of residential mobility data may have limited the power to detect an effect on intima-media thickness.

Factores de riesgo cardiovascular dependientes de la infección por VIH / HIV-related cardiovascular risk factors

Diversas evidencias procedentes de estudios experimentales y observacionales sugieren que la infección por el virus de la inmunodeficiencia humana (VIH) per se y el estado proinflamatorio asociado pueden aumentar el riesgo de enfermedad cardiovascular. La infección por VIH puede activar diversas vías inflamatorias de la pared vascular con liberación de citocinas y expresión de moléculas de adhesión endotelial. El tratamiento antirretroviral de gran actividad (TARGA) es capaz de suprimir muchas de estas alteraciones. El papel del VIH en el riesgo cardiovascular se ha puesto de manifiesto en los estudios de interrupción de tratamiento, fundamentalmente en el estudio SMART, en el que se demostró una mayor mortalidad cardiovascular en el grupo que interrumpía el TARGA. El cambio brusco a un estado más proinflamatorio producido por la reanudación repentina de la replicación viral podría inducir un aumento de la adhesión plaquetaria y la migración de células inflamatorias con inestabilización de la placa. Algunos estudios sugieren que el VIH puede producir también daño endotelial y se ha descrito un descenso de los marcadores de activación endotelial y una mejoría de la función endotelial tras el inicio del TARGA, que se ha correlacionado con el descenso de la carga viral del VIH. Finalmente, el VIH podría inducir enfermedad cardiovascular a través de su efecto sobre el colesterol unido a lipoproteínas de alta densidad que puede descender en pacientes con infección no controlada. Aunque la relación del VHC con el riesgo cardiovascular es controvertida, la coinfección por el VHC se ha asociado con una mayor frecuencia de resistencia insulínica y de infarto agudo de miocardio en algunas cohortes

Evidence from experimental and observational studies suggests that HIV infection per se and the associated proinflammatory state can increase the risk of cardiovascular disease. HIV infection can activate several inflammatory pathways in the vascular wall with cytokine release and expression of endothelial adhesion molecules. Many of these alterations can be suppressed by highly-active antiretroviral therapy (HAART). The role of HIV in cardiovascular risk has been demonstrated in studies of treatment interruption, mainly in the SMART trial, in which greater cardiovascular mortality was observed in the group interrupting HAART. The abrupt change to a more proinflammatory state produced by sudden resumption of viral replication could induce an increase in platelet adhesion and migration of inflammatory cells with plaque instability. Some studies suggest that HIV can also produce endothelial damage; a decrease in markers of endothelial activation and improvement of endothelial function after initiation of HAART have been described, and these changes have been correlated with the decrease in HIV viral load. Finally, HIV can induce cardiovascular disease through its effect on high-density lipoprotein cholesterol, which can decrease in patients with uncontrolled infection. Although the association of HIV with cardiovascular risk is controversial, coinfection with hepatitis C infection has been associated with a higher frequency of insulin resistance and acute myocardial infarction in some cohorts

Factores de riesgo cardiovascular dependientes del tratamiento antirretroviral / Cardiovascular risk factors associated with antiretroviral therapy

Los pacientes infectados por el virus de la inmunodeficiencia humana (VIH) comparten los factores de riesgo cardiovascular tradicionales con la población general. Además, el propio VIH incrementa significativamente el riesgo de enfermedad cardiovascular. Por este motivo, el control de la infección por el VIH con tratamiento antirretroviral de gran actividad (TARGA) ayuda a reducir el riesgo vascular de los pacientes infectados por el VIH. Hay evidencias de que el TARGA incrementa el riesgo cardiovascular, y se ha asociado el uso de abacavir, ddI, lopinavir/r e indinavir con el desarrollo de infarto agudo de miocardio (IAM). Sin embargo, el riesgo absoluto de desarrollar IAM en pacientes que reciben TARGA es muy bajo con relación al alto beneficio obtenido por la terapia antirretroviral

HIV-infected patients share traditional cardiovascular risk factors with the general population. Moreover, HIV per se significantly increases the risk of cardiovascular disease. Consequently, control of HIV infection with highly-active antiretroviral therapy (HAART) helps to reduce vascular risk in HIV-infected patients. However, there is evidence that HAART increases cardiovascular risk and the use of abacavir, didanosine, lopinavir/ritonavir and indinavir has been associated with the development of acute myocardial infarction (AMI). However, the absolute risk of AMI in patients receiving HAART is very low in relation to the benefit obtained with antiretroviral therapy